Unit 1: CV System Part D

Question 1

Unlike skeletal muscle, cardiac muscle..

Answer 1

does NOT require a stimulus from the nervous system in order to contract

Question 2

Cardiac Muscle Cells split

Answer 2

Cardiac Muscle Cells
–> Modified/Specialized = Intrinsic Conduction System
–> Autorhythmic cells - generate APs OR –> Conducting cells

Cardiac Muscle Cells
–> “Normal” = Myocardium –> Contractile cells

Question 3

Conduction System

Answer 3

Composed of non-contractile (no sarcomeres) cardiac cells that generate and conduct action potentials

Question 4

What are the 2 parts of the Conduction System?

Answer 4

a. Autorhythmic pacemaker cells
- SA node
- AV node

b. Conducting cells
-Interatrial pathway
- internodal pathway
- AV bundle
- purkinjie fibers

Question 5

Sinoatrial (SA) Node

Answer 5

Ø In right atrium

Ø generates action potentials (APs) at a rate of 100 APs/min (modified by parasympathetic (PSNS) innervation to be 75 APs/min at rest)

Ø generates action potentials faster than other areas of the heart, therefore acts as the natural pacemaker of the heart

Question 6

Atrioventricular (AV) node

Answer 6

Ø in right atrium

Ø generates action potentials at a rate of 50 APs/min

Ø Composed of small diameter cells with few gap junctions that slow down the AP conduction speed

Creates ~100 msec delay in AP conduction that ensures the atria contract and are fully empty before ventricular contraction begins

Question 7

The rate of APs of both SA and AV nodes are influenced by…

Answer 7

the nervous and endocrine systems

Allows changes in heart for activities like exercise, sleep, etc

Question 8

Conducting cells

Answer 8

large diameter conducting cells (can be autorhythmic)

Question 9

Interatrial pathway

Answer 9

Carries signals from SA node to left atrium

Question 10

internodal pathway

Answer 10

Carries signals from SA node to AV node

Question 11

Atrioventricular (AV) bundle

Answer 11

Ø only pathway through which APs are carried from atria to ventricles.

Ø Carries signal quickly through ventricular septum where bundle splits into two branches (Bundle Branches) that carry the signal to the apex of heart

Question 12

Purkinje Fibers

Answer 12

also known as ”subendocardial conducting network”

Ø Network of terminal branches that transmit impulses (action potentials) to contractile cells.

Question 13

What happens if the the SA node is damaged?

Answer 13

If the SA node is damaged, the atria may not contract and action potentials in the heart will be
produced at the rate of the AV node (50 APs/min). This may not be high enough to sustain life
functions. In this case, a manmade pacemaker (consisting of a battery and electrode) can be surgically
implanted under the skin to artificially stimulate the AV node cells at a rate that is within normal range.

Question 14

Describe the mechanisms by which action potentials are generated in myocardial autorhythmic cells

Answer 14

These cells produce unstable membrane potentials called pacemaker potentials that are capable of spontaneously producing action potentials

Unlike neurons and skeletal muscle cells, these cells
have no resting membrane potential and a threshold of -40mV.

a. Pacemaker potential
- I f (funny) channels open, and Na+ enters the cell causing a slow depolarization toward threshold.

b. Depolarization phase
- At threshold, I f (funny) channels close (no more Na+ entry), and voltage gated Ca++ channels open. Calcium enters cell quickly (cell becomes more and more positive).

c. Repolarization phase
-At peak, voltage gated Ca++ channels close, slow K + channels open. K + exits the cells, decreasing membrane potential.

• At -60mV, voltage gated K + channels close, I f channels reopen, and the next
  pacemaker potential begins (results in a continuous cycle of action potentials)

Question 15

Describe the mechanisms by which action potentials are generated in myocardial contractile cells

Answer 15

a. Phase 4: Resting Membrane Potential
- Is -90mv in contractile cardiac cells

b. Phase 0: Depolarization phase
- Depolarization of autorhythmic cells spreads through gap junctions to contractile cells. Voltage gated Na+ channels open; Na+ enters cell until membrane is depolarized to +20 mV.

c. Phase 1: Initial Repolarization Phase
- Na+ channels close, fast K+ channels open, K+ leaves cell causing repolarization.

d. Phase 2: Plateau
-Voltage gated Ca++ channels open, fast K+ channels close. Ca++ entry and decreased permeability to K+ prolongs depolarization.

e. Phase 3: Repolarization phase
- Voltage gated slow K+ channels open, K+ exits cell and membrane potential returns to resting levels

Question 16

Explain the significance of the plateau phase in the action potential of a cardiac contractile cell.

Answer 16

The Absolute refractory period is almost as long as the contractile response (contraction + relaxation)

The long absolute refractory period ensures that a second contraction cannot be initiated before the first has completed. I.e. summation and tetanus are prevented. Allows for alternation of contraction and relaxation of the myocardium with enough time in between beats for the chambers to fill with blood (i.e. heartbeat)

Question 17

Describe or diagram excitation-contraction coupling in cardiac muscle

Answer 17

a. Contractile cell depolarizes and action potential on sarcolemma travels down T-tubules and triggers….

b. Opening of voltage gated Ca++ channels (L-type calcium channels) on the membrane (T-tubule). Calcium enters the cell.

c. Ca++ binds to ryanodine receptor (RyR) Ca++ release channel on the membrane of the sarcoplasmic reticulum (SR).

d. RyR channel opens and Ca++ is released into the cytosol. This process is described as Ca++ induced Ca++ release., which leads to a Ca++ signal.

e. Ca++ ions bind to troponin, initiating the contraction cycle and crossbridge formation (myosin binds to actin, powerstroke, etc).

f. Relaxation of the cell involves: Ca ++ ATPase pumping Ca++ into the SR. Na+/ Ca++ Exchanger (NCX), an antiport that moves Ca++ out of cell in exchange for Na+. As Ca++ levels in the cytosol decrease,
Ca++ unbinds from troponin, stopping the contraction cycle